BEC hydrochloride is a slow-binding and competitive Arginase II inhibitor with Ki of 0.31 μM (ph 7.5).target: Arginase II [1];In vitro: BEC hydrochloride causes significant enhancement of NO-dependent smooth muscle relaxation in this tissue. [2] BEC hydrochloride enhances perivascular and peribronchiolar lung inflammation, mucus metaplasia, NF-κB DNA binding, and mRNA expression of the NF-κB-driven chemokine genes CCL20 and KC, and lead to further increases in airways hyperresponsiveness. [3] In vivo: BEC hydrochloride increased contractility in isolated myocytes from WT and NOS3 but not NOS1 knockout mice. [4]
References:
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[2]. Kim NN et al. Probing erectile function: S-(2-boronoethyl)-L-cysteine binds to arginase as a transition state analogue and enhances smooth muscle relaxation in human penile corpus cavernosum. Biochemistry. 2001 Mar 6;40(9):2678-88.
[3]. Karina Ckless et al. Inhibition of Arginase Activity Enhances Inflammation in Mice with Allergic Airway Disease, in Association with Increases in Protein S-Nitrosylation and Tyrosine Nitration. J Immunol. Author manuscript; available in PMC 2010 Jun 28.
[4]. Steppan J et al. Arginase modulates myocardial contractility by a nitric oxide synthase 1-dependent mechanism. Proc Natl Acad Sci U S A. 2006 Mar 21;103(12):4759-64.